Etiology of Periodontal Disease

Periodontal diseases are considered multi-factorial inflammatory diseases of a host-

bacterial interaction. Their development and progression depend on the complex
interrelationship between many local and systemic predisposing factors.

Etiology of periodontal disease can be broadly classified to

1-Primary (Initiating factor)
2-Secondary (modifying factor)
In addition to Absence of beneficial bacteria.

In health there is equilibrium between aggression of bacterial plaque and reparative

tissue capacity. This equilibrium could be broken by increased amount or virulence
of bacteria or decreased defensive capacity of tissue.

Primary (Initiating factor)

Microbial dental plaque:
Within hours after birth, the sterile oral cavity is colonized by low numbers of mainly
facultative and aerobic bacteria. The number of oral bacteria increases gradually as
a result of exposure to external environmental microbial sources.

After tooth eruption, a more complex oral microbiota is established

It is estimated that the oral bacterial microbiome of adults encompasses

approximately 700 commonly occurring species, approximately half of which can
be present at any time in any individual.

When one thinks about bacteria, one almost immediately associates them with
different pathologic conditions. However, most oral bacteria are harmless
commensals under normal circumstances. This means that this microbiota lives in
harmony with its host but that, under specific conditions (i.e., increased mass and/or
pathogenicity, suppression of commensal or beneficial bacteria, and/ or reduced host
response), disease can occur.

It is generally accepted that the primary etiology of periodontal diseases is

bacterial plaque. The composition of dental plaque varies considerably among
patients and among sites in the same patient.

Dental plaque is a structured, resilient, yellow-grayish complex microbial

community (predominantly bacteria, but it may contain yeast, protozoa and virus)
found on the tooth and other oral surfaces, embedded in a matrix of bacterial and
salivary origin, so firmly adherent to tooth surface that they resist wash off by
salivary flow.

Plaque develops naturally on teeth, and forms part of the defense systems of the host
by helping to prevent colonization of enamel by exogenous (and often pathogenic)
microorganisms (colonization resistance).

Tooth surface and can form complex bacterial communities that may harbor over
500 distinct species and contain over 1010 bacteria per mg.

Plaque may be differentiated from other deposits that may be found on the tooth
surface such as a materia alba and calculus;

o Materia alba; is a soft accumulation of bacteria and tissue cells that lack the
organized structure of dental plaque and are easily displaced with a water spray.

o Calculus; is a hard deposit that forms by mineralization of dental plaque and is

generally covered by a layer of un-mineralized plaque.

➢ Types of dental plaque:

Plaque is divided into 2 distinct types based on the relationship of the plaque to the
gingival margin:

1. Supragingival plaque
2. Subgingival plaque
Supragingival plaque Subgingival plaque
Above the gingival margin and can be Below the gingival margin, between the tooth
further sub divided into and the gingival pocket epithelium
o Coronal: on the tooth surface
o Marginal: immediate contact with o Subgingival plaque subdivided into:
the gingival margin. - Tooth associated
- Tissue associated
- Apical bacteria lying free within the
pocket
- Supragingival plaque is subject to
much more oral abrasion, which - In contrast to supragingival plaques,
restrict its net accumulation. subgingival biofilm residing in a more
protected location not subjected to intraoral
- Supragingival biofilm is subject to abrasion or salivary host defense components.
the flow characteristics of saliva, and
its host defense components such as;
• IgA
• Lactoferrin
• Lysozyme
• Peroxidases
All has a wide antimicrobial activity
and serve to limit both colonization
and spread of biofilm.
A) Tooth associated: or attached plaque is
Supragingival plaque Dominated by: characterized by gram positive rods and cocci
such as:
• Gram +ve facultative cocci - Streptococcus mitis
and rods mainly streptococci - Streptococcus sanguis
and Actinomyces species - Actinomyces viscosus
- Actinomyces naeslundii

B) Tissue associated: Bacteria in this areas are

more loosely organized than the very dense
tooth associated region. Mostly predominate
bacteria include;
- Prophyromonas gingivalis
- Prevotella intermedia
- Aggregatibacter actinomycitim cometans
- Capnocytophaga
 ➢ Dental plaque composition
1. Cells
2. Intracellular matrix

1. Cells
In addition to the bacterial cells, plaque contains a small number of Epithelial cells,
leukocytes, macrophages.

2. Intracellular matrix
The intercellular matrix consists of organic and inorganic materials derived from
saliva, gingival crevicular fluid, and bacterial products.

• Organic constituents of the matrix include polysaccharides produced by

bacteria, proteins, glycoproteins from the saliva, lipid material from the
membranes of disrupted bacterial and host cells, and DNA.

• The inorganic components of plaque are predominantly calcium and

phosphorus, with trace amounts of other minerals. The source of inorganic
constituents of supragingival plaque is primarily saliva. As the mineral
content increases, the plaque mass becomes calcified to form calculus. The
inorganic components of subgingival plaque are derived from crevicular fluid.

➢ MECHANISMS OF PLAQUE FORMATION

1. Formation of acquired pellicle

2. Bacterial adherence

3. Formation of intermicrobial matrix

4. Bacterial colonization and plaque maturation

5.Dispersion
 1. Formation of acquired pellicle:

All surfaces in the oral cavity, including the hard and soft tissues, are coated with a
layer of organic material known as the acquired pellicle.

The salivary pellicle can be detected on clean enamel surfaces within the first few
hours by adsorption of salivary proteins and glycoprotein, together with some
bacterial molecules to the tooth surface.

The pellicle is effectively the tooth's skin and protects it from acids. However,
bacteria can also attach to the pellicle, which sometimes leads to plaque formation.

The pellicle on tooth surfaces consists of more than 180 peptides, proteins, and
glycoproteins, including keratins, mucins, proline-rich proteins, phosphoproteins,
histidine-rich proteins, and other molecules that can function as adhesion sites
(receptors) for bacteria

The pellicle-coated tooth surface is colonized by Gram-positive bacteria (Primary

colonizers) such as:
• Streptococcus sanguis
• streptococcus gordonii
• Streptococcus mutans
• Actinomyces viscosus
• actionomyces naeslundii
• Neisseria

Importance of acquired pellicle in plaque formation:

a) Acquired pellicle provides specific receptors for bacterial attachment. Ex;
streptococcus gordonii and actionomyces naeslundii, two initial colonizers bind
acidic proline rich proteins found in the pellicle by lock and key mechanism.
b) It provide surface for additional bacterial attachment, by
- co aggregation: the ability of the two genetically identical bacteria to adhere to
one another ex; attachment between gram positive cocci and rods.
- co-adhesion: Surface receptors on the gram positive cocci and rods allow the
subsequent adherence of gram negative organisms which have poor ability to
directly adhere to the pellicle.
c) Supply of growth substrates for secondary colonizers
d) Reduce oxygen tension to the low level required for growth and survival of
anaerobic secondary colonizers

2. Bacterial adherence

The single most important phenomenon in the development of a biofilm is the

process of microbial adhesion either to the substratum or to other adhering cells of
the same or another species.

The initial steps in colonization of teeth by bacteria occur in three phases. Phase 1 is
transport to the surface, phase 2 is initial reversible adhesion, and phase 3 is strong
irreversible attachment.

Phase 1: Transport to the Surface

The first stage involves the initial transport of the bacterium to the tooth surface.
Random contacts may occur, for example, through sedimentation of
microorganisms, or through active bacterial movement. However, relatively few oral
bacteria are motile, and forces such as saliva flow or mechanical contact between
oral soft tissues and teeth are almost certainly more important than swimming for
bringing the primary colonizing bacteria into contact with teeth.

Phase 2: Initial Adhesion

The second stage results in an initial reversible adhesion of the bacterium.
These interactions are essentially nonspecific. Reversible week attractive force
between microbial cell surfaces and the acquired pellicle occur via electrostatic and
hydrophobic interactions.

Phase 3: Strong Attachment

After initial adhesion, a firm anchorage between the bacterium and the surface is
established. The specific interactions include Irreversible adhesion that occur
between microbial cell surface “adhesin” molecules (fimbiria) and receptors in the
salivary pellicle’s glycoprotein (e.g. proline-rich proteins)
This type of adhesion will determine whether a bacterial cell will remain associated
with the surface or not. Only a relatively small proportion of oral bacteria possess
adhesins that interact with receptors in the host pellicle, and these organisms are
generally the most abundant bacteria in biofilms on tooth enamel.

Irreversible adhesion also may occur by the synthesis of extracellluler polymers such
as, soluble and insoluble high molecular weight polysaccharides synthesized from
sucrose (Levan and glucans)

- The primary colonizers provide new binding sites for adhesion by other oral
bacteria. The metabolic activity of the primary colonizers modifies the local
microenvironment in ways that can influence the ability of other bacteria to survive
in the dental plaque biofilm. For example, by removing oxygen, the primary
colonizers provide conditions of low oxygen tension that permit the survival and
growth of obligate anaerobes.

3. Formation of intermicrobial matrix

Organic substances formed by bacterial enzymes from sucrose, they are mainly
polysaccharides of:

• Glucans: mainly dextran which is a sticky adhesive material that plays a

major role in colonization of bacteria
• Levans: Levan function as storage of polysaccharide, providing an energy
source when hydrolyzed.
• Mutan: Non degradable, act as skeleton and play a rule in irreversible
adhesion.

4. Bacterial colonization and plaque maturation :

• Division of the attached cells
• Secondary colonizers
• Tertiary colonizers
• Plaque maturation and concept of biofilm
Division of the attached Secondary colonizers Tertiary colonizers
cells
Division of the attached Mature plaque mass After one week of plaque
cells to produce creating an oxygen accumulation, other Gram-
confluent growth. deprived environment negative species may also
dominated by gram be present in plaque. These
negative anaerobic species represent what is
microorganisms which considered to be the
contribute to an increased "tertiary colonizers"
pathogeneicty of the
plaque biofilm.
Outgrowth Once The secondary colonizers
attached, pioneer species include Gram-negative • Porphyromonas
multiply. The forming species such as: gingivalis
microcolony spreads first • Fusobacterium • Campylobacter
in the plane of the surface nucleatum, rectus,
and then, as space • Prevotella • Eikenella
becomes limited, intermedia, and corrodens,
upwards creating • Capnocytophaga • Aggregatibacter
palisades of cells. species. actinomycetem
comitans,

The transition from early supragingival dental plaque to mature plaque growing
below the gingival margin involves a shift in the microbial population from primarily
gram-positive organisms to high numbers of gram-negative bacteria.

5- Dispersion:
When biofilm is established plankotic (free) bacteria can detach either by rolling,
detach on clumps or swarming and seeding, and rapidly multiply and disperse.
 ➢ Dental plaque as a biofilm:
It has been recognized that sessile microbial populations were considered to be
sufficiently different from free-living microorganisms to merit their own name, and
the term biofilms was coined. Biofilms are barriers that composed of microbial cells
encased within a matrix of extracellular polymeric substances, such as
polysaccharides, proteins, and nucleic acids.

Dental plaque are excellent examples of biofilm communities. Bacteria exist,

interact and proliferate within the Gel like intercellular matrix increasing the
concentration of bacterial products, which in turn used for metabolic interactions
among bacteria.

• The structure of bacterial biofilm contains areas of high and low

bacterial masses connected with aqueous channels of different sizes.

• These channels provide nutrients for bacterial colonies and facilitate the
movement of metabolic waste products within the colony.

• Bacteria in a biofilm are not distributed evenly. They are grouped in

micro colonies surrounded by an enveloping intermicrobial matrix.

• Biofilm protects bacteria from harmful substances such as anti-bacterial

agents, and allow the bacteria to be 1000 times more resistant to
antimicrobial agents than their free floating counterparts.

Properties of biofilm (READING ONLY)

1- Interactions Among Dental Plaque Bacteria
• Lactate and formate are byproducts of streptococci and actinomyces
and may be utilized in the metabolism of other bacteria such as
veillonella and campylobacter.

• Growth of Porphyromonas gingivalis (Pg) is enhanced by metabolic

products produced by other organisms such as succinate from
capnocytophaga and Campylobacter species, and Menadione
byproduct of veillonella species.
 • Hemin iron which result from breakdown of host heamoglobins
important in metabolism of Pg.

• Antagonistic interactions include the production of inhibitory

substances such as bacteriocins, H2O2, and organic acids.

• Early bacterial colonizers streptococci and actinomyces utilizes oxygen

and lowers the reduction oxidation potential of the environment which
favor the growth of anaerobic species.

2- Communication Between Biofilm Bacteria

• Bacterial cells do not exist in isolation. In a biofilm, bacteria have the

capacity to communicate with each other. One example of this is
quorum sensing. Bacteria in biofilms communicate through these
signaling molecules, and use this "quorum-sensing" system to optimize
their virulence factors and survival.

• Bacteria secrete a signaling molecule that accumulates in the local

environment and triggers a response such as a change in the expression
of specific genes once they reach a critical threshold concentration. The
threshold concentration is reached only at a high cell density, and
therefore bacteria sense that the population has reached a critical mass
or quorum.

3- Biofilms and Antimicrobial Resistance

• Bacteria growing in microbial communities’ adherent to a surface do

not “behave” the same way as bacteria growing suspended in a liquid
environment (planktonic). For example, the resistance of bacteria to
antimicrobial agents is dramatically increased in the biofilm. Almost
without exception, organisms in a biofilm are 1000 to 1500 times more
resistant as compared with antibiotics in their planktonic state. The
mechanisms of this increased resistance differ from species to species,
from antibiotic to antibiotic, and for biofilms growing in different
habitats.
 ➢ Factors That Affect Supragingival Dental Plaque Formation:

1- Topography of Supragingival Plaque

Early plaque formation on teeth follows a typical topographic pattern, with initial
growth along the gingival margin and from the interdental spaces (i.e., the areas
protected from shear forces). Later, a further extension in the coronal direction can
be observed.
This pattern may change severely when the tooth surface contains irregularities that
offer a favorable growth path.

2- Surface Microroughness
Rough intraoral surfaces (e.g., crown margins, implant abutments, denture bases)
accumulate and retain more plaque and calculus.

3- Individual Variables That Influence Plaque Formation

The rate of plaque formation differs significantly among subjects. Some patients
considered to be “heavy” (fast) plaque formers while others considered as “light”
(slow) plaque formers.

4- Variation Within the Dentition

Within a dental arch, large differences in plaque growth rate can be detected. In
general, early plaque formation occurs faster: in the lower jaw (as compared with
the upper jaw); in molar areas; on the buccal tooth surfaces (as compared with palatal
sites, especially in the upper jaw); and in the interdental regions (as compared with
the buccal or lingual surfaces).

5- Impact of Gingival Inflammation and Saliva

Several studies clearly indicate that early in vivo plaque formation is more rapid on
tooth surfaces facing inflamed gingival margins than on those adjacent to healthy
gingivae.

6- Impact of Patient’s Age

Reports clearly indicate that a subject’s age does not influence de novo plaque
formation. However, the developed plaque in the older patient group resulted in
more severe gingival inflammation, which seems to indicate an increased
susceptibility to gingivitis with aging.